Article : Study Suggests Way to Prevent Heart Failure

Discussion in 'Health and medical' started by e = \( r e u B e n \) ², Oct 3, 2003.

  1. WASHINGTON (Reuters) - Researchers said on Wednesday they had found a
    possible new way to treat and prevent heart failure -- a chronic and often
    deadly condition that affects 4.9 million Americans and millions more around
    the world.
    The international study focuses on a gene that makes heart cells susceptible
    to the effects of adrenaline, a hormone that goes into overdrive in heart

    Heart failure develops when the heart is stressed, usually by heart disease
    or high blood pressure but sometimes by an infection. The heart stops
    pumping efficiently and becomes more and more damaged as it works harder to
    get blood in and out.

    While the latest work has only been done so far in mice, it suggests a new
    approach to heart failure, which kills half of its victims within five

    "Despite newer therapies to treat heart failure, patient mortality rates
    remain high, indicating a need for novel treatment strategies that
    complement current methods," said Dr. Howard Rockman, a professor of
    medicine at Duke University in North Carolina who led the study.

    He said the study also provides insights into how chronic high blood
    pressure, for instance, can cause heart failure.

    Patients often take a cocktail of drugs, including beta-blockers and ACE
    inhibitors to control high blood pressure and diuretics to lower the amount
    of fluid the heart is working to pump.

    Writing in the Journal of Clinical Investigation, Rockman and colleagues
    said they targeted beta-adrenergic receptors on the surface of heart cells.
    These molecular doorways help control a cell's response to adrenaline.

    In heart failure patients, the constant stress causes the body to produce
    more and more adrenaline. These beta-adrenergic receptors become
    over-stimulated and in time stop responding.

    Rockman's team had earlier identified a protein called PI3Kgamma that, when
    disrupted, helps maintain the beta-adrenergic receptors on heart cells even
    after chronic stimulation by adrenaline.

    They genetically engineered mice to produce an inactive form of PI3Kgamma.
    These mice had active beta-adrenergic receptors even after constant doses of
    an adrenaline-like chemical, the researchers reported. Normal mice exposed
    to the chemical developed symptoms of heart failure.

    "These findings identify a potential new target for heart drugs and may have
    important clinical implications," Rockman said.